miR-4486 enhances cisplatin sensitivity of gastric cancer cells by restraining the JAK3/STAT3 signalling pathway

Zhou, Caijin; Chen, Linxia; Chen, Rihong; Xu, Feipeng; Huang, Zhe; Huang, Ruxun; Wang, Weiwei; Xu, Qianqian

doi:10.1080/1120009x.2021.1936957

Cited by 10 publications

(5 citation statements)

References 42 publications

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“…One functionally validated target of miR-4486 is JAK3, which was also identified in our analysis as an upstream regulator significantly associated with differentially methylated transcripts in SARS-CoV-2-infected cells ( Fig. 5 and 6C ) ( 44 ). One possible hypothesis based on our network analysis is that degradation of JAK3 transcript by miR-4486 leads to lower STAT3 activation as a compensatory mechanism in the infected cell to counteract SARS-CoV-2-induced STAT3 hyperactivation ( Fig.…”

Section: Discussionmentioning

confidence: 52%

Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

et al. 2023

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Posttranscriptional modification of viral and cellular RNA by N 6 -methyladenosine (m 6 A) plays an important role in regulating the replication of many viruses and the cellular immune response to infection. We therefore sought to define the epitranscriptomic m 6 A profile of human lung epithelial cells infected with SARS-CoV-2.

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Section: Discussionmentioning

confidence: 52%

Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

et al. 2023

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“…One functionally validated target of miR-4486 is JAK3, which was also identified in our analysis as an upstream regulator significantly associated with differentially methylated transcripts in SARS-CoV-2-infected cells (Figs. 4 and 5C) (Zhou et al, 2022). One possible hypothesis based on our network analysis is that degradation of JAK3 transcript by miR-4486 leads to lower STAT3 activation as a compensatory mechanism in the infected cell to counteract SARS-CoV-2-induced STAT3 hyperactivation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Epitranscriptomic N⁶-methyladenosine profile of SARS-CoV-2-infected human lung epithelial cells

Phillips

Khadka

Bohan

et al. 2022

Preprint

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N6-methyladenosine (m6A) is a dynamic post-transcriptional RNA modification that plays an important role in determining transcript fate. Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) has caused the global pandemic of coronavirus disease 2019 (COVID-19) and the virus has been extensively studied. However, how m6A modification of host cell RNAs change during SARS-CoV-2 infection has not been reported. Here we define the epitranscriptomic m6A profile of SARS-CoV-2-infected human lung epithelial cells compared to uninfected controls. Biological pathway analyses revealed that differentially methylated transcripts were significantly associated with cancer-related pathways, protein processing in the endoplasmic reticulum, cell death and proliferation. Upstream regulators predicted to be associated with the proteins encoded by differentially methylated mRNAs include proteins involved in the type I interferon response, inflammation, and cytokine signaling. These data suggest that m6A modification of cellular RNA is an important mechanism of regulating host gene expression during SARS-CoV-2 infection of lung epithelial cells.

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“…To explore the relationship of PIK3CD and other genes/signaling pathways in GC, we performed correlation analyses of 415 GC samples from TCGA database using LinkedOmics (http://www.linkedomics.org/login.php). Notably, we found that the expression of PIK3CD is positively associated with JAK3 (R = 0.8432, p < 0.05), a kind of Janus tyrosine kinase that has been wildly reported to promote cancer progression [24][25][26][27] (Figure 6A). Importantly, the expression of PIK3CD is also positively associated with the expression levels of STAT5A (R = 0.5139, p < 0.05) and STAT5B (R = 0.4794, p < 0.05), two downstream genes of JAK3 signaling (Figure 6B).…”

Section: Jak3/stat5 Signaling Activates Pik3cd Expression In Gcmentioning

confidence: 93%

JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

Hu,

Dou,

et al. 2024

Journal of Cell Communication and Signaling

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Gastric cancer (GC) is one of the most common solid cancers with high incidence and mortality worldwide. Chronic gastritis and consequent inflammatory microenvironment is known as a major cause leading to gastric carcinogenesis. Here we report that PIK3CD that encodes p110δ, a catalytic subunit of the class IA PI3Ks, is overexpressed and tumorigenic in GC and associated with tumor inflammatory microenvironment. By investigating the data from TCGA database and our immunohistochemical staining and quantitative real‐time PCR results from clinical samples, we found PIK3CD exhibits higher expression level in GC tissues compared with adjacent non‐tumorous stomach tissues. Genetic silencing of PIK3CD in GC cells retards proliferation and migration in vitro and tumorigenicity and metastasis in vivo. In contrast, enhanced expression of PIK3CD promotes these phenotypes in vitro. Furthermore, pharmacological inhibition of PIK3CD could reduce GC cell viability and colony formation capacities. More importantly, we reveal a relevant mechanism that PIK3CD, but not PIK3CA and PIK3CB, is transcriptionally regulated by the pro‐inflammatory IL2/JAK3/STAT5 axis and tumor‐infiltrating immune cells such as lymphocytes. These observations may setup a new crosstalk between tumor inflammatory microenvironment, IL2/JAK3/STAT5 signaling and PI3K/AKT signaling. Targeting PIK3CD may be a promising therapy strategy for GC.

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miR-4486 enhances cisplatin sensitivity of gastric cancer cells by restraining the JAK3/STAT3 signalling pathway

Cited by 10 publications

References 42 publications

Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N⁶-methyladenosine profile of SARS-CoV-2-infected human lung epithelial cells

JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

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miR-4486 enhances cisplatin sensitivity of gastric cancer cells by restraining the JAK3/STAT3 signalling pathway

Cited by 10 publications

References 42 publications

Epitranscriptomic N 6 -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N 6 -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N6-methyladenosine profile of SARS-CoV-2-infected human lung epithelial cells

JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

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Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Epitranscriptomic N⁶-methyladenosine profile of SARS-CoV-2-infected human lung epithelial cells